Unveiling the stealthy tactics: mycoplasma's immune evasion strategies.

Mycoplasmas, the smallest known self-replicating organisms, possess a simple structure, lack a cell wall, and have limited metabolic pathways. They are responsible for causing acute or chronic infections in humans and animals, with a significant number of species exhibiting pathogenicity. Although the innate and adaptive immune responses can effectively combat this pathogen, mycoplasmas are capable of persisting in the host, indicating that the immune system fails to eliminate them completely. Recent studies have shed light on the intricate and sophisticated defense mechanisms developed by mycoplasmas during their long-term co-evolution with the host. These evasion strategies encompass various tactics, including invasion, biofilm formation, and modulation of immune responses, such as inhibition of immune cell activity, suppression of immune cell function, and resistance against immune molecules. Additionally, antigen variation and molecular mimicry are also crucial immune evasion strategies. This review comprehensively summarizes the evasion mechanisms employed by mycoplasmas, providing valuable insights into the pathogenesis of mycoplasma infections.

Annexin A2: the missing piece in the puzzle of pathogen-induced damage.

Annexin A2 is a Ca2+ regulated protein belonging to the Annexin family and is found in the cytoplasm and cell membrane. It can exist in a monomeric form or in a heterotetrameric form with the S100A10 dimer. The research on Annexin A2 in tumours is currently active, and studies on its role in pathogen infection are increasing. Annexin A2 plays a crucial role in the life cycle of viruses by mediating adhesion, internalization, uncoating, transport, and release. In the case of parasites, bacteria, mycoplasma, fungi, and other pathogens, Annexin A2 binds to the ligand on the pathogen, which mediates the pathogen's adhesion to the host cell, ultimately leading to infection and damage to the host. Furthermore, some studies have developed biological or chemical drugs that target Annexin A2, which have demonstrated promising anti-infective effects. Thus, targeting Annexin A2 may present a promising therapeutic approach for the treatment of diverse infectious diseases. In summary, this paper provides an overview of Annexin A2 and its role in various pathogens. It highlights its regulation of pathogen infection and its potential as a therapeutic target for the treatment of infectious diseases.

Pushing the envelope: Immune mechanism and application landscape of macrophage-activating lipopeptide-2.

Mycoplasma fermentans can cause respiratory diseases, arthritis, genitourinary tract infections, and chronic fatigue syndrome and have been linked to the development of the human immunodeficiency virus. Because mycoplasma lacks a cell wall, its outer membrane lipoproteins are one of the main factors that induce inflammation in the organism and contribute to disease development. Macrophage-activating lipopeptide-2 (MALP-2) modulates the inflammatory response of monocytes/macrophages in a bidirectional fashion, indirectly enhances the cytotoxicity of NK cells, promotes oxidative bursts in neutrophils, upregulates surface markers on lymphocytes, enhances antigen presentation on dendritic cells and induces immune inflammatory responses in sebocytes and mesenchymal cells. MALP-2 is a promising vaccine adjuvant for this application. It also promotes vascular healing and regeneration, accelerates wound and bone healing, suppresses tumors and metastasis, and reduces lung infections and inflammation. MALP-2 has a simple structure, is easy to synthesize, and has promising prospects for clinical application. Therefore, this paper reviews the mechanisms of MALP-2 activation in immune cells, focusing on the application of MALP-2 in animals/humans to provide a basis for the study of pathogenesis in Mycoplasma fermentans and the translation of MALP-2 into clinical applications.

Comparison of the median effective concentration (EC50) and effect of sevoflurane with or without remifentanil in cesarean section with supreme laryngeal mask under narcotrend monitoring: a randomized trial.

BACKGROUND: Remifentanil combined with sevoflurane is a standard protocol for obstetric general anesthesia (GA). METHODS: In this study, we performed a randomized clinical trial to evaluate whether remifentanil has an effect on the median effective concentration (EC50) of sevoflurane and compare anesthetic outcomes of them in cesarean section with Supreme™ laryngeal mask airway (SLMA) under narcotrend monitoring. Ninety parturients with singleton births undergoing elective cesarean delivery (CD) with initial inhaled 1.0 minimum alveolar concentration (MAC) sevoflurane for anesthesia maintenance were assigned to three groups randomly and evenly: Group A (0.05 µg·kg-1·min-1 remifentanil combined with sevoflurane), Group B (0.1 µg·kg-1·min-1 remifentanil combined with sevoflurane), and Group C (normal saline combined with sevoflurane). Narcotrend was used to monitor the depth of anesthesia during the operation, with the level of anesthesia depth controlled within the D-E stage. The EC50 of sevoflurane was determined by Dixon's sequential method. The Narcotrend index, amount of bleeding, neonatal Apgar score, and corresponding treatment measures in the three groups were recorded. RESULTS: The results showed that the estimated EC50 of sevoflurane for obstetric GA was 0.80 MAC (95% CI: 0.63-0.95 MAC) in group A, 0.82 MAC (95% CI: 0.63-0.96 MAC) in group B, and 0.80 MAC (95% CI: 0.63-0.95 MAC) in group C. There was no statistically significant difference in the estimated EC50 of sevoflurane, time to wakefulness, Apgar score, amount of intraoperative bleeding, and postoperative bleeding within 24 hours between the three groups (all P>0.05). CONCLUSIONS: The addition of remifentanil at 0.05-0.1 µg·kg-1·min-1 did not change the EC50 of sevoflurane and anesthetic quality. The concentration of inhaled anesthetics can be minimized with Narcotrend monitoring. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR2000034512.